Homeostatic Regulation of the Vascular System

Homeostatic Regulation ofthe Vascular System Bởi: OpenStaxCollege In order to maintain homeostasis in the cardiovascular system and provide adequate blood to the tissues, blood flow must

Homeostatic Regulation of

the Vascular System

Bởi:

OpenStaxCollege

In order to maintain homeostasis in the cardiovascular system and provide adequate blood to the tissues, blood flow must be redirected continually to the tissues as they become more active In a very real sense, the cardiovascular system engages in resource allocation, because there is not enough blood flow to distribute blood equally to all tissues simultaneously For example, when an individual is exercising, more blood will

be directed to skeletal muscles, the heart, and the lungs Following a meal, more blood is directed to the digestive system Only the brain receives a more or less constant supply

of blood whether you are active, resting, thinking, or engaged in any other activity

[link]provides the distribution of systemic blood at rest and during exercise Although most of the data appears logical, the values for the distribution of blood to the integument may seem surprising During exercise, the body distributes more blood to the body surface where it can dissipate the excess heat generated by increased activity into the environment

Systemic Blood Flow During Rest, Mild Exercise, and

Maximal Exercise in a Healthy Young Individual

Organ

Resting (mL/

min)

Mild exercise (mL/

min)

Maximal exercise (mL/ min)

Systemic Blood Flow During Rest, Mild Exercise, and

Maximal Exercise in a Healthy Young Individual

Organ

Resting (mL/

min)

Mild exercise (mL/

min)

Maximal exercise (mL/ min) Others

Three homeostatic mechanisms ensure adequate blood flow, blood pressure, distribution, and ultimately perfusion: neural, endocrine, and autoregulatory mechanisms They are summarized in[link]

Summary of Factors Maintaining Vascular Homeostasis Adequate blood flow, blood pressure, distribution, and perfusion involve autoregulatory, neural,

and endocrine mechanisms.

Neural Regulation

The nervous system plays a critical role in the regulation of vascular homeostasis The primary regulatory sites include the cardiovascular centers in the brain that control both

cardiac and vascular functions In addition, more generalized neural responses from the limbic system and the autonomic nervous system are factors

The Cardiovascular Centers in the Brain

Neurological regulation of blood pressure and flow depends on the cardiovascular centers located in the medulla oblongata This cluster of neurons responds to changes in blood pressure as well as blood concentrations of oxygen, carbon dioxide, and hydrogen ions The cardiovascular center contains three distinct paired components:

• The cardioaccelerator centers stimulate cardiac function by regulating heart rate and stroke volume via sympathetic stimulation from the cardiac accelerator nerve

• The cardioinhibitor centers slow cardiac function by decreasing heart rate and stroke volume via parasympathetic stimulation from the vagus nerve

• The vasomotor centers control vessel tone or contraction of the smooth muscle

in the tunica media Changes in diameter affect peripheral resistance, pressure, and flow, which affect cardiac output The majority of these neurons act via the release of the neurotransmitter norepinephrine from sympathetic neurons

Although each center functions independently, they are not anatomically distinct

There is also a small population of neurons that control vasodilation in the vessels of the brain and skeletal muscles by relaxing the smooth muscle fibers in the vessel tunics Many of these are cholinergic neurons, that is, they release acetylcholine, which in turn stimulates the vessels’ endothelial cells to release nitric oxide (NO), which causes vasodilation Others release norepinephrine that binds to β2 receptors A few neurons release NO directly as a neurotransmitter

Recall that mild stimulation of the skeletal muscles maintains muscle tone A similar phenomenon occurs with vascular tone in vessels As noted earlier, arterioles are normally partially constricted: With maximal stimulation, their radius may be reduced to one-half of the resting state Full dilation of most arterioles requires that this sympathetic stimulation be suppressed When it is, an arteriole can expand by as much as 150 percent Such a significant increase can dramatically affect resistance, pressure, and flow

Baroreceptor Reflexes

Baroreceptors are specialized stretch receptors located within thin areas of blood vessels and heart chambers that respond to the degree of stretch caused by the presence of blood They send impulses to the cardiovascular center to regulate blood pressure Vascular baroreceptors are found primarily in sinuses (small cavities) within the aorta and carotid

arteries: The aortic sinuses are found in the walls of the ascending aorta just superior

to the aortic valve, whereas the carotid sinuses are in the base of the internal carotid arteries There are also low-pressure baroreceptors located in the walls of the venae cavae and right atrium

When blood pressure increases, the baroreceptors are stretched more tightly and initiate action potentials at a higher rate At lower blood pressures, the degree of stretch is lower and the rate of firing is slower When the cardiovascular center in the medulla oblongata receives this input, it triggers a reflex that maintains homeostasis ([link]):

• When blood pressure rises too high, the baroreceptors fire at a higher rate and trigger parasympathetic stimulation of the heart As a result, cardiac output falls Sympathetic stimulation of the peripheral arterioles will also decrease, resulting in vasodilation Combined, these activities cause blood pressure to fall

• When blood pressure drops too low, the rate of baroreceptor firing decreases This will trigger an increase in sympathetic stimulation of the heart, causing cardiac output to increase It will also trigger sympathetic stimulation of the peripheral vessels, resulting in vasoconstriction Combined, these activities cause blood pressure to rise

Baroreceptor Reflexes for Maintaining Vascular Homeostasis Increased blood pressure results in increased rates of baroreceptor firing, whereas decreased blood pressure results in slower rates of fire, both initiating the homeostatic mechanism to

restore blood pressure.

The baroreceptors in the venae cavae and right atrium monitor blood pressure as the blood returns to the heart from the systemic circulation Normally, blood flow into the aorta is the same as blood flow back into the right atrium If blood is returning to the right atrium more rapidly than it is being ejected from the left ventricle, the atrial receptors will stimulate the cardiovascular centers to increase sympathetic firing and increase cardiac output until homeostasis is achieved The opposite is also true This mechanism is referred to as the atrial reflex

Chemoreceptor Reflexes

In addition to the baroreceptors are chemoreceptors that monitor levels of oxygen, carbon dioxide, and hydrogen ions (pH), and thereby contribute to vascular homeostasis Chemoreceptors monitoring the blood are located in close proximity to the baroreceptors in the aortic and carotid sinuses They signal the cardiovascular center as well as the respiratory centers in the medulla oblongata

Since tissues consume oxygen and produce carbon dioxide and acids as waste products, when the body is more active, oxygen levels fall and carbon dioxide levels rise as cells undergo cellular respiration to meet the energy needs of activities This causes more hydrogen ions to be produced, causing the blood pH to drop When the body is resting, oxygen levels are higher, carbon dioxide levels are lower, more hydrogen is bound, and

pH rises (Seek additional content for more detail about pH.)

The chemoreceptors respond to increasing carbon dioxide and hydrogen ion levels (falling pH) by stimulating the cardioaccelerator and vasomotor centers, increasing cardiac output and constricting peripheral vessels The cardioinhibitor centers are suppressed With falling carbon dioxide and hydrogen ion levels (increasing pH), the cardioinhibitor centers are stimulated, and the cardioaccelerator and vasomotor centers are suppressed, decreasing cardiac output and causing peripheral vasodilation In order

to maintain adequate supplies of oxygen to the cells and remove waste products such as carbon dioxide, it is essential that the respiratory system respond to changing metabolic demands In turn, the cardiovascular system will transport these gases to the lungs for exchange, again in accordance with metabolic demands This interrelationship of cardiovascular and respiratory control cannot be overemphasized

Other neural mechanisms can also have a significant impact on cardiovascular function These include the limbic system that links physiological responses to psychological stimuli, as well as generalized sympathetic and parasympathetic stimulation

Endocrine Regulation

Endocrine control over the cardiovascular system involves the catecholamines, epinephrine and norepinephrine, as well as several hormones that interact with the kidneys in the regulation of blood volume

Epinephrine and Norepinephrine

The catecholamines epinephrine and norepinephrine are released by the adrenal medulla, and enhance and extend the body’s sympathetic or “fight-or-flight” response (see [link]) They increase heart rate and force of contraction, while temporarily constricting blood vessels to organs not essential for flight-or-fight responses and redirecting blood flow to the liver, muscles, and heart

Antidiuretic Hormone

Antidiuretic hormone (ADH), also known as vasopressin, is secreted by the cells in the hypothalamus and transported via the hypothalamic-hypophyseal tracts to the posterior pituitary where it is stored until released upon nervous stimulation The primary trigger prompting the hypothalamus to release ADH is increasing osmolarity of tissue fluid, usually in response to significant loss of blood volume ADH signals its target cells in the kidneys to reabsorb more water, thus preventing the loss of additional fluid in the urine This will increase overall fluid levels and help restore blood volume and pressure

In addition, ADH constricts peripheral vessels

Renin-Angiotensin-Aldosterone Mechanism

The renin-angiotensin-aldosterone mechanism has a major effect upon the cardiovascular system ([link]) Renin is an enzyme, although because of its importance

in the renin-angiotensin-aldosterone pathway, some sources identify it as a hormone Specialized cells in the kidneys found in the juxtaglomerular apparatus respond to decreased blood flow by secreting renin into the blood Renin converts the plasma protein angiotensinogen, which is produced by the liver, into its active form—angiotensin I Angiotensin I circulates in the blood and is then converted into angiotensin II in the lungs This reaction is catalyzed by the enzyme angiotensin-converting enzyme (ACE)

Angiotensin II is a powerful vasoconstrictor, greatly increasing blood pressure It also stimulates the release of ADH and aldosterone, a hormone produced by the adrenal cortex Aldosterone increases the reabsorption of sodium into the blood by the kidneys Since water follows sodium, this increases the reabsorption of water This in turn increases blood volume, raising blood pressure Angiotensin II also stimulates the thirst

center in the hypothalamus, so an individual will likely consume more fluids, again increasing blood volume and pressure

Hormones Involved in Renal Control of Blood Pressure

In the renin-angiotensin-aldosterone mechanism, increasing angiotensin II will stimulate the production of antidiuretic hormone and aldosterone In addition to renin, the kidneys produce erythropoietin, which stimulates the production of red blood cells, further increasing blood

volume.

Erythropoietin

Erythropoietin (EPO) is released by the kidneys when blood flow and/or oxygen levels decrease EPO stimulates the production of erythrocytes within the bone marrow Erythrocytes are the major formed element of the blood and may contribute 40 percent

or more to blood volume, a significant factor of viscosity, resistance, pressure, and flow

In addition, EPO is a vasoconstrictor Overproduction of EPO or excessive intake of synthetic EPO, often to enhance athletic performance, will increase viscosity, resistance, and pressure, and decrease flow in addition to its contribution as a vasoconstrictor

Atrial Natriuretic Hormone

Secreted by cells in the atria of the heart, atrial natriuretic hormone (ANH) (also known

as atrial natriuretic peptide) is secreted when blood volume is high enough to cause extreme stretching of the cardiac cells Cells in the ventricle produce a hormone with similar effects, called B-type natriuretic hormone Natriuretic hormones are antagonists

to angiotensin II They promote loss of sodium and water from the kidneys, and suppress renin, aldosterone, and ADH production and release All of these actions promote loss

of fluid from the body, so blood volume and blood pressure drop

Autoregulation of Perfusion

As the name would suggest, autoregulation mechanisms require neither specialized nervous stimulation nor endocrine control Rather, these are local, self-regulatory mechanisms that allow each region of tissue to adjust its blood flow—and thus its perfusion These local mechanisms include chemical signals and myogenic controls

Chemical Signals Involved in Autoregulation

Chemical signals work at the level of the precapillary sphincters to trigger either constriction or relaxation As you know, opening a precapillary sphincter allows blood

to flow into that particular capillary, whereas constricting a precapillary sphincter temporarily shuts off blood flow to that region The factors involved in regulating the precapillary sphincters include the following:

• Opening of the sphincter is triggered in response to decreased oxygen

concentrations; increased carbon dioxide concentrations; increasing levels of lactic acid or other byproducts of cellular metabolism; increasing

concentrations of potassium ions or hydrogen ions (falling pH); inflammatory chemicals such as histamines; and increased body temperature These

conditions in turn stimulate the release of NO, a powerful vasodilator, from endothelial cells (see[link])

• Contraction of the precapillary sphincter is triggered by the opposite levels of the regulators, which prompt the release of endothelins, powerful

vasoconstricting peptides secreted by endothelial cells Platelet secretions and certain prostaglandins may also trigger constriction

Again, these factors alter tissue perfusion via their effects on the precapillary sphincter mechanism, which regulates blood flow to capillaries Since the amount of blood is limited, not all capillaries can fill at once, so blood flow is allocated based upon the needs and metabolic state of the tissues as reflected in these parameters Bear in mind, however, that dilation and constriction of the arterioles feeding the capillary beds is the primary control mechanism

The Myogenic Response

The myogenic response is a reaction to the stretching of the smooth muscle in the walls

of arterioles as changes in blood flow occur through the vessel This may be viewed

as a largely protective function against dramatic fluctuations in blood pressure and blood flow to maintain homeostasis If perfusion of an organ is too low (ischemia), the tissue will experience low levels of oxygen (hypoxia) In contrast, excessive perfusion could damage the organ’s smaller and more fragile vessels The myogenic response is a

localized process that serves to stabilize blood flow in the capillary network that follows that arteriole

When blood flow is low, the vessel’s smooth muscle will be only minimally stretched

In response, it relaxes, allowing the vessel to dilate and thereby increase the movement

of blood into the tissue When blood flow is too high, the smooth muscle will contract in response to the increased stretch, prompting vasoconstriction that reduces blood flow [link]summarizes the effects of nervous, endocrine, and local controls on arterioles

Summary of Mechanisms Regulating Arteriole Smooth Muscle and Veins